However, in several cancers, MYC/c-MYC genes and those downstream of signaling pathways that stimulate cell proliferation almost always become overexpressed through mutations in the MYC/c-MYC gene or, more commonly, by induction of its expression due to activation of an upstream gene (e.g., ERK), or by its life extension due to mutations, such as that in the Thr58 phosphorylation site, which reduce the efficiency of its phosphorylation-dependent ubiquitination. This evidence concerns the gene MAPK1 and cancer.